Congestive heart failure (CHF) is a group of symptoms (or symptom complex) due to the heart not being able to adequately pump blood to meet the demands of the body/tissues. A result of this inability to adequately pump blood is that the tissues behind the pump (i.e., the lungs with respect to the left ventricle) becomes congested or filled with excess fluid, hence the name congestive heart failure. As blood backs up behind the left ventricle, the lungs become engorged and stiff with the patient complaining of shortness of breath. If the right ventricle fails, the backed-up blood causes the organs in the abdomen to become engorged with blood, and also causes the legs to become swollen. As the heart's ability to pump blood progressively decreases, the patient becomes increasingly more tired and fatigued.
Congestive heart failure can be due to any number of causes, such as dilated cardiomyopathy, hypertrophic cardiomyopathy, valvular dysfunction or volume overload with a normal heart as in chronic renal failure. Among these known causes, only dilated cardiomyopathy is treated with cardiomyoplasty. For the purpose of this patent application, congestive heart failure as used herein will mean congestive heart failure due to dilated cardiomyopathy.
The causes of congestive heart failure are multiple. In the United States and Europe, the most common cause is coronary artery disease resulting in myocardial infarctions (heart attacks) which destroy a portion of the heart muscle, thereby weakening the heart. The heart may also be affected by a vital or other infections (such as Trypanosoma cruzi, most common in South America), toxins (the most common of which is alcohol), or unknown causes (referred to as "idiopathic"). It is estimated that there are over 100,000 new patients each year with congestive heart failure.
At the present time, the therapy for congestive heart failure is primarily pharmacological, with some major recent success utilizing the angiotensin converting enzyme (ACE) inhibitors. However, the use of ACE inhibitors does not correct the problem; it only treats it. Hence, the basic pathophysiologic process continues, and eventually pharmacological therapy will be ineffective.
A popular therapy for advanced congestive heart failure, particularly in younger individuals, is cardiac transplant. However, this therapy is very limited because it requires a major surgical procedure, is very expensive, and acceptable donor hearts are in very limited supply. Hence, what is needed is a more viable therapy for advanced congestive heart failure.
In recent years, it has been postulated that strong skeletal muscle tissue could be trained to repeatedly contract, and yet not fatigue. If such "trained" muscle tissue were translocated within a patient so that it were wrapped around the failing heart, then such translocated muscle tissue could assist, if not take over for, the failing cardiac muscle tissue, thereby allowing the heart to better perform its function of a pump. The idea is that when the stronger skeletal muscle tissue contracts, after it has been wrapped around the heart, it compresses the heart from the outside, thereby augmenting the vigor with which the heart ejects (pumps) blood. Such translocation of skeletal or other strong muscle tissue around the heart is referred to as "cardiac myopiasty".
Cardiac myopiasty offers the advantage of avoiding some of the more common and serious problems associated with cardiac transplant, namely a limited supply of donor hearts, rejection of the donated heart, or infection due to the immunosuppressive agents used to prevent rejection. Advantageously, there is almost always some healthy skeletal or other muscle tissue of the patient that may be translocated and wrapped around the patient's heart. Thus, unlike transplanted hearts (which are in limited supply; are usually only located after diligent searching and long waiting; and, when found, must still be safely transported to a medical facility where the transplant operation can take place), the skeletal or other muscle tissue is with the patient at all times. Further, because the translocated muscle tissue is the patient's own tissue, there is no risk of rejection, as commonly occurs when a heart is transplanted. Using translocated muscle tissue also eliminates the need for lifetime pharmacological therapy with agents designed to prevent rejection, yet which agents have a high incidence of side effects (such as atherosclerosis, altered post-immunocompetence resulting in infection and malignancy). Such agents also tend to be very expensive. Hence, cardiac myopiasty offers a very attractive alternative to cardiac transplant. In order for cardiac myopiasty to be a viable option for a patient suffering from congestive heart failure, there is a need in the art for a quick and safe method or technique of training the muscle tissue that has been translocated around the heart. Such training of the muscle tissue involves repetitive stimulation of the muscle tissue with a stimulation device, e.g., a pulse generator.
Heretofore, such stimulation of the muscle tissue has involved two different pacing modes. Initially, to "train" the muscle, a pulse generator has been used with the stimulating electrode in contact with either the muscle or the neurovascular bundle supplying the muscle. The muscle tissue is then stimulated by delivering output pulses at progressively more rapid rates over a period of weeks. After such initial training, the muscle tissue is translocated so as to be wrapped around the heart. The tissue is then stimulated with a dual-chamber pulse generator. One channel of the dual-chamber pulse generator is used for cardiac sensing and pacing and is electrically connected to either the ventricle or the atrium using either a conventional endocardial or myocardial lead. The other channel is electrically connected to the translocated muscle tissue using, either myocardial or intramuscular lead(s).
There are two types of pulse generators currently in use to provide the dual-chamber stimulation: a demand-type "DDD" pacemaker, and a dedicated cardiac myostimulator. A myostimulator sytem typically comprises a first intramuscular lead near the nerve branches of the translocated muscle tissue, a second intramuscular lead placed distal from the first to act as the anode, and a third lead for sensing native depolarizations of the heart.
Unfortunately, there are several disadvantages associated with using a myostimulator system to train the translocated muscle tissue. First, such system requires a special purpose pulse generator designed to deliver burst pacing. Second, such burst pacing rapidly depletes the battery longevity of the device, causing it to have a relatively short life. Third, the size, weight and cost of the myostimulator device is very high.
The other type of dual-chamber pulse generator currently used to stimulate the translocated muscle tissue is the demand-type DDD pacemaker. Such dual-chamber pacemaker is configured such that one channel (the atrial channel) senses the native depolarization of the atrium (or paces the atrium, as required), and the other channel paces the translocated muscle tissue one AV delay thereafter. Thus, the synchronization delay is the dual-chamber pacemaker's programmed AV interval, and is set equal to the patient's native PR interval. Thus, as the atrium contracts or is stimulated, the dual-chamber pacemaker issues a stimulation pulse one AV interval thereafter, thereby stimulating the translocated muscle tissue at approximately the same time that the ventricle contracts. In this way, the strong skeletal muscle tissue is stimulated to squeeze the ventricle, helping to eject or pump the blood, in synchrony with the heart's natural rhythm.
Disadvantageously, the use of a dual-chamber pulse generator to stimulate the translocated muscle tissue in the above-described manner suffers from many of the same drawbacks as using a myostimulator pulse generator, i.e., the size, weight and cost of a dual-chamber pulse generator is very high.
In addition, in a patient with congestive heart failure, the failing ventricle may cause a backup in pressure which, in turn, may cause a high pressure buildup in the atria, and may cause the atria to dilate. When this occurs, a very common response is atrial fibrillation, which is a very rapid and disorganized (ineffective) rhythm of the atria. Such rapid atrial rhythm is not a coordinated rhythm and is contraindicated for dual-chamber pacing. Hence, the dual-chamber DDD pacemaker (which is able to sense the atrial contractions) has no way to determine a reference point from which to measure the AV interval, and is accordingly not able to properly synchronize the stimulation of the translocated skeletal tissue with the ventricular contraction. In addition, patients with congestive heart failure have frequent ectopic ventricular beats which are not coordinated with native atrial activity.
What is needed, therefore, is a device that can effectively train translocated muscle tissue, does not require a dual-chamber pulse generator; has a long life; has a size, weight and cost that is significantly less than that of either dual-chamber pulse generators or myostimulator devices, and does not induce any other type of arrhythmias.
Thus, there is a need in the art for a technique of stimulating translocated muscle tissue placed around the heart in a coordinated manner in synchrony with the ventricle's natural rhythm.